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A role for endogenous glucocorticoids in wound repair

Richard Grose, Silke Werner, Daniela Kessler, Jan Tuckermann, Katharina Huggel, Silke Durka, Holger M Reichardt, Sabine Werner

Author Affiliations

  1. Richard Grose14,
  2. Silke Werner1,
  3. Daniela Kessler2,
  4. Jan Tuckermann3,
  5. Katharina Huggel1,
  6. Silke Durka1,
  7. Holger M Reichardt35 and
  8. Sabine Werner*,1
  1. 1 Institute of Cell Biology, Department of Biology, ETH Zürich, CH‐8093, Zürich, Switzerland
  2. 2 Department of Dermatology, University of Cologne, D‐50925, Cologne, Germany
  3. 3 Division of Molecular Biology of the Cell I, German Cancer Research Centre, D‐69120, Heidelberg, Germany
  4. 4 Cancer Research UK, London Research Institute, London, WC2A 3PX, UK
  5. 5 Institute of Virology and Immunobiology, University of Würzburg, D‐97078, Würzburg, Germany
  1. *Corresponding author. Tel: +41 1 633 3941; Fax: +41 1 633 1174; E-mail: Sabine.werner{at}cell.biol.ethz.ch
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Abstract

Exogenous glucocorticoids are known to inhibit wound repair, but the roles and mechanisms of action of endogenous glucocorticoids during the healing process are as yet unknown. Therefore, we wounded mice expressing a DNA‐binding‐defective mutant version of the glucocorticoid receptor (GRdim mice) and also analysed fibroblasts from these animals in vitro. We found a remarkably enlarged granulation tissue with a high fibroblast density in GRdim mice. This difference is likely to result from an increased migratory and proliferative capacity of GRdim fibroblasts and from elevated expression levels of soluble factors involved in granulation tissue formation in wounds of GRdim mice. In spite of the larger granulation tissue seen in early wounds, late wounds appeared normal, most likely due to an enhanced ability of GRdim fibroblasts to contract collagen. These results demonstrate an as yet unidentified role of endogenous glucocorticoids in the regulation of wound repair.

  • Received February 20, 2002.
  • Revision received April 29, 2002.
  • Accepted April 30, 2002.
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